Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

5.0K
Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
5.0K
T Cell Types and Functions01:24

T Cell Types and Functions

627
When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
627
IP3/DAG Signaling Pathway01:11

IP3/DAG Signaling Pathway

11.5K
Membrane lipids such as phosphatidylinositol (PI) are precursors for several membrane-bound and soluble second messengers. Specific kinases phosphorylate PI and produce phosphorylated inositol phospholipids. One such inositol phospholipids are the  phosphatidylinositol-4,5 bisphosphate [PI(4,5)P2], present in the inner half of the lipid bilayer. Upon ligand binding, GPCR stimulates Gq proteins to turn on phospholipase Cꞵ. Activated phospholipase Cꞵ cleaves PI(4,5)P2 and...
11.5K
Inflammatory Response01:28

Inflammatory Response

1.6K
An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
1.6K
GPCR Desensitization01:12

GPCR Desensitization

5.6K
G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...
5.6K
Asthma-II: Pathophysiology and Classification01:26

Asthma-II: Pathophysiology and Classification

2.6K
Asthma is a prevalent chronic respiratory condition marked by inflammation and hyperresponsiveness of the airways. Its pathophysiology involves complex interactions among inflammatory pathways, immune responses, and neural mechanisms.
Additionally, environmental and genetic factors play crucial roles in determining an individual's susceptibility to asthma and the severity of their condition.
Critical processes in asthma pathophysiology include:
2.6K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

The Explosion of Life: Lessons from Live Imaging of Ovulation.

Reproduction (Cambridge, England)·2026
Same author

Characterizing individual differences in SCR responsivity: A hybrid mixture and single-trial modeling framework.

Biological psychology·2026
Same author

Deployment-Related Respiratory Health: Bridging the Gap between Clinical and Epidemiological Associations and Disease Mechanisms An Official American Thoracic Society Workshop Report.

Annals of the American Thoracic Society·2026
Same author

Adipose tissue as a site of immune activation and dysfunction in individuals with obesity and asthma.

bioRxiv : the preprint server for biology·2026
Same author

Outcomes of Lung Transplantation for Pulmonary Sarcoidosis Across Multiple Eras: A 25-Year Experience from a US Center.

Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG·2026
Same author

Critical illness expands a transcriptionally distinct hypometabolic CD8<sup>+</sup> T effector program associated with respiratory failure and mortality.

bioRxiv : the preprint server for biology·2026

Related Experiment Video

Updated: May 12, 2025

Isolation of Group 2 Innate Lymphoid Cells from Mouse Nasal Mucosa to Detect the Expression of CD226
08:30

Isolation of Group 2 Innate Lymphoid Cells from Mouse Nasal Mucosa to Detect the Expression of CD226

Published on: May 10, 2022

1.8K

PGI2 restricts trained ILC2 responses in allergic inflammation.

Weisong Zhou1, Jian Zhang1, Allison E Norlander2

  • 1Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, TN, United States.

Journal of Immunology (Baltimore, Md. : 1950)
|May 7, 2025
PubMed
Summary

Prostaglandin I2 (PGI2) signaling inhibits trained immunity in pulmonary type 2 innate lymphoid cells (ILC2s). Blocking this pathway enhances allergic inflammation and IL-13 production in ILC2s.

Keywords:
ILC2inflammationlungmouse

More Related Videos

Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy
10:39

Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy

Published on: April 16, 2019

7.6K
Adoptive Immunotherapy of iNKT Cells in Glucose-6-Phosphate Isomerase G6PI-Induced RA Mice
08:43

Adoptive Immunotherapy of iNKT Cells in Glucose-6-Phosphate Isomerase G6PI-Induced RA Mice

Published on: January 31, 2020

6.7K

Related Experiment Videos

Last Updated: May 12, 2025

Isolation of Group 2 Innate Lymphoid Cells from Mouse Nasal Mucosa to Detect the Expression of CD226
08:30

Isolation of Group 2 Innate Lymphoid Cells from Mouse Nasal Mucosa to Detect the Expression of CD226

Published on: May 10, 2022

1.8K
Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy
10:39

Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy

Published on: April 16, 2019

7.6K
Adoptive Immunotherapy of iNKT Cells in Glucose-6-Phosphate Isomerase G6PI-Induced RA Mice
08:43

Adoptive Immunotherapy of iNKT Cells in Glucose-6-Phosphate Isomerase G6PI-Induced RA Mice

Published on: January 31, 2020

6.7K

Area of Science:

  • Immunology
  • Allergy Research
  • Innate Immunity

Background:

  • Pulmonary type 2 innate lymphoid cells (ILC2s) develop immune memory, known as trained immunity, enhancing responses to subsequent allergen exposures.
  • The role of prostaglandin I2 (PGI2), a cyclooxygenase (COX) metabolite, and its receptor IP in modulating trained ILC2 responses is not well understood.

Purpose of the Study:

  • To investigate the hypothesis that IP signaling inhibits ILC2 training.
  • To elucidate the function of PGI2 in trained innate immunity within the lung.

Main Methods:

  • Utilized a mouse model to induce ILC2 training using Alternaria alternata extract.
  • Compared wild-type (WT) and IP knockout (KO) mice following a secondary challenge with papain, an unrelated allergen.
  • Analyzed lung immune cell populations, cytokine expression (IL-13), and gene expression profiles (RNA sequencing) of ILC2s.

Main Results:

  • IP knockout mice exhibited significantly heightened ILC2 IL-13 expression and lung eosinophilia after papain challenge compared to WT mice.
  • Augmented type 2 inflammation in IP KO mice correlated with increased numbers and IL-13 production by ILC2s.
  • RNA sequencing revealed heightened immune response and mitochondrial pathways in IP-deficient ILC2s, indicating enhanced activation.

Conclusions:

  • PGI2 signaling plays an inhibitory role in trained ILC2 responses.
  • IP signaling is a key regulator of innate immune memory and allergic inflammation in the lungs.